2-Deoxy-D-glucose (2-DG)

Catalog No.S4701 Synonyms: 2-deoxyglucose, NSC 15193, 2-Deoxy-D-arabino-hexose, D-Arabino-2-deoxyhexose

For research use only.

2-Deoxy-D-glucose (2-DG, 2-deoxyglucose, NSC 15193, 2-Deoxy-D-arabino-hexose, D-Arabino-2-deoxyhexose), an analog of glucose, is a glycolytic inhibitor with antiviral activity. 2-Deoxy-D-glucose induces apoptosis and inhibits Herpes Simplex Virus type-1 (HSV-1) receptor expression.

2-Deoxy-D-glucose (2-DG) Chemical Structure

CAS No. 154-17-6

Selleck's 2-Deoxy-D-glucose (2-DG) has been cited by 35 publications

Purity & Quality Control

Choose Selective Carbohydrate Metabolism Inhibitors

Biological Activity

Description 2-Deoxy-D-glucose (2-DG, 2-deoxyglucose, NSC 15193, 2-Deoxy-D-arabino-hexose, D-Arabino-2-deoxyhexose), an analog of glucose, is a glycolytic inhibitor with antiviral activity. 2-Deoxy-D-glucose induces apoptosis and inhibits Herpes Simplex Virus type-1 (HSV-1) receptor expression.
Targets
glycolysis [1]
In vitro

2-Deoxy-D-glucose(2-DG) activates AKT function through phosphatidylinositol 3-kinase (PI3K) and is independent of glycolysis or mTOR inhibition. 2-DG treatments disrupts the binding between insulin-like growth factor 1 (IGF-1) and IGF-binding protein 3 (IGFBP3) so that the free form of IGF-1 could be released from the IGF-1·IGFBP3 complex to activate IGF-1 receptor (IGF1R) signaling. 2-DG-induced activation of many survival pathways can be jointly attenuated through IGF1R inhibition. 2-DG also induces time- and dose-dependent ERK phosphorylation[1]. 2-DG is readily transported into cells and is phosphorylated by hexokinase, but cannot be metabolized further and accumulates in the cell. This leads to ATP depletion and the induction of cell-death[2]. 2DG significantly suppresses proliferation, causes apoptosis and reduces migration of murine endothelial cells, inhibiting formation of lamellipodia and filopodia and causing disorganization of F-actin filaments in murine endothelial cell[5].

In vivo Treatment of cancer patients with relatively high doses of 2-DG (greater than 200 mg/kg) was largely ineffective in managing tumor growth. Side effects of 2-DG included elevated blood glucose levels, progressive weight loss with lethargy, and behavioral symptoms of hypoglycemia[2]. 2-DG enhances isoflurane-induced loss of righting reflex in mice. By reducing metabolism, 2-DG treatment can decrease body temperature in rodent, enhancing sensitivity to anesthetics[3]. 2-DG diet significantly increased serum ketone body level and brain expression of enzymes required for ketone body metabolism. The 2-DG-induced maintenance of mitochondrial bioenergetics was paralleled by simultaneous reduction in oxidative stress. Further, 2-DG treated mice exhibited a significant reduction of both amyloid precursor protein (APP) and amyloid beta (Aβ) oligomers, which was paralleled by significantly increased α-secretase and decreased γ-secretase expression, indicating that 2-DG induced a shift towards a non-amyloidogenic pathway. 2-DG increased expression of genes involved in Aβ clearance pathways, degradation, sequestering, and transport. Concomitant with increased bioenergetic capacity and reduced β-amyloid burden, 2-DG significantly increased expression of neurotrophic growth factors, BDNF and NGF, thus reduces pathology in female mouse model of Alzheimer's disease[4].

Protocol (from reference)

Cell Research:

[1]

  • Cell lines: H460 or H157 cells
  • Concentrations: 5 mM
  • Incubation Time: 48 h
  • Method:

    2×103 H460 or H157 cells are seeded in 96-well cell culture plates. Cells are treated with 5 mM 2-DG only, 5 or 10 μM IGF1R inhibitor II only, or a combination of 2-DG and IGF1R inhibitor II. Cell growth inhibition is determined after 48 h by the CellTiter 96® AQueous nonradioactive cell proliferation assay.

Animal Research:

[3]

  • Animal Models: Adult C57BL/6J mice
  • Dosages: 1000 mg/kg
  • Administration: i.p.

Solubility (25°C)

In vitro

DMSO 32 mg/mL
(194.93 mM)
Water 32 mg/mL
(194.93 mM)
Ethanol ''1 mg/mL

Chemical Information

Molecular Weight 164.16
Formula

C6H12O5

CAS No. 154-17-6
Storage 3 years -20°C powder
2 years -80°C in solvent
Smiles C(C=O)C(C(C(CO)O)O)O

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Molarity Calculator

Mass Concentration Volume Molecular Weight

Clinical Trial Information

NCT Number Recruitment Interventions Conditions Sponsor/Collaborators Start Date Phases
NCT02558140 Completed Biological: RO6874813 Neoplasms Hoffmann-La Roche October 11 2015 Phase 1
NCT01998841 Active not recruiting Drug: Crenezumab|Drug: Placebo Alzheimer''s Disease Genentech Inc.|Banner Alzheimer''s Institute|National Institute on Aging (NIA) December 20 2013 Phase 2

(data from https://clinicaltrials.gov, updated on 2022-01-17)

Tech Support

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